Preprint Review Version 1 This version is not peer-reviewed

The role of miR-29a in the regulation, function, and signaling of liver fibrosis

Version 1 : Received: 10 June 2018 / Approved: 11 June 2018 / Online: 11 June 2018 (14:03:48 CEST)

A peer-reviewed article of this Preprint also exists.

Huang, Y.-H.; Yang, Y.-L.; Wang, F.-S. The Role of miR-29a in the Regulation, Function, and Signaling of Liver Fibrosis. Int. J. Mol. Sci. 2018, 19, 1889. Huang, Y.-H.; Yang, Y.-L.; Wang, F.-S. The Role of miR-29a in the Regulation, Function, and Signaling of Liver Fibrosis. Int. J. Mol. Sci. 2018, 19, 1889.

Journal reference: Int. J. Mol. Sci. 2018, 19, 1889
DOI: 10.3390/ijms19071889

Abstract

Both fibrosis and cirrhosis of the liver are the end results of most kinds of chronic liver damage and present a common but difficult clinical challenge throughout the world. The inhibition of the fibrogenic, proliferative, and migratory effects of hepatic stellate cells (HSCs) has become an experimental therapy for preventing and even reversing hepatic fibrosis. Furthermore, a complete understanding of the function of non-coding RNA-mediated epigenetic mechanisms in HSC activation may improve our perception of liver fibrosis pathogenesis. This review focuses on an evolving view of molecular mechanisms in which HSC activation by miR-29a signaling may moderate their profibrogenic phenotype, thus supporting the use of miR-29a agonists as a potential therapy for treating liver fibrosis in the future.

Subject Areas

miR-29a; cholestasis; apoptosis; ER stress; toll like receptors; epigenetics

Comments (0)

We encourage comments and feedback from a broad range of readers. See criteria for comments and our diversity statement.

Leave a public comment
Send a private comment to the author(s)
Views 0
Downloads 0
Comments 0
Metrics 0


×
Alerts
Notify me about updates to this article or when a peer-reviewed version is published.